Management of NSAID/Aspirin-Induced Small Intestinal Damage by GI-Sparing NSAIDs, Anti-Ulcer Drugs and Food Constituents

Satoh, Hiroshi; Takeuchi, Koji

doi:10.2174/092986712803413980

Cited by 32 publications

(19 citation statements)

References 73 publications

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“…The severity of indomethacin-induced small intestinal damage was reduced by several antiulcer drugs, such as lafutidine, irsogladine, rebamipide, and teprenone [35,36,37,38,39,40]. The effects of irsogladine were particularly potent and mimicked by rolipram, an inhibitor of phosphodiestrease (PDE) type IV, through a mechanism that is thought to be associated with an increase in the secretion of mucus [35].…”

Section: Effects Of Various Drugs On Nsaid-induced Small Intestinal Dmentioning

confidence: 99%

“…No satisfactory means for the treatment of NSAID-induced enteropathy are currently available for patients. This situation has been markedly intensified by the recent findings that antisecretory drugs, such as PPIs and H 2 -RAs, are ineffective against NSAID-induced small intestinal damage [37,38] and even worsen the severity of these lesions [41,42,43]. Furthermore, it was also found that soluble dietary fibers protect the small intestine against NSAID-induced damage, probably by compensating for a decreased in barrier function caused by NSAIDs.…”

Section: Summary and Future Prospectsmentioning

confidence: 99%

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NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

Takeuchi

Satoh²

2015

Digestion

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Background/Aims: NSAID-induced enteropathy has been the focus of recent basic and clinical research subsequent to the development of the capsule endoscope and double-balloon endoscope. We review the possible pathogenic mechanisms underlying NSAID-induced enteropathy and discuss the role of the inhibition of COX-1/COX-2 and the influences of food as well as various prophylactic treatments on these lesions. Methods: Studies were performed in experimental animals. Results: Multiple factors, such as intestinal hypermotility, decreased mucus secretion, enterobacteria, and upregulation of iNOS/NO expression, are involved in the pathogenesis of NSAID-induced enteropathy, in addition to the decreased production of PGs due to the inhibition of COX. Enterobacterial invasion is the most important pathogenic event, and intestinal hypermotility, which was associated with this event, is essential for the development of these lesions. NSAIDs also upregulate the expression of COX-2, and the inhibition of both COX-1 and COX-2 is required for the intestinal ulcerogenic properties of NSAIDs to manifest. NSAID-induced enteropathy is prevented by PGE₂, atropine, ampicillin, and aminoguanidine as well as soluble dietary fiber, and exacerbated by antisecretory drugs such as proton pump inhibitors. Conclusion: These findings on the pathogenesis of NSAID-induced enteropathy will be useful for the future development of intestinal-sparing alternatives to standard NSAIDs.

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Section: Effects Of Various Drugs On Nsaid-induced Small Intestinal Dmentioning

confidence: 99%

Section: Summary and Future Prospectsmentioning

confidence: 99%

NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

Takeuchi

Satoh²

2015

Digestion

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“…Один из таких препаратов -ре-бамипид (мукоген). Ребамипид (0,1 per os 3 р/д) стимулирует образование Pg, «очищает» слизистую от свободных радикалов и таким образом способ-ствует защите слизистой желудка [7,44,53].…”

Section: нивелирование дефицита простагландиновunclassified

Preventive and therapeutic strategies of pharmaco-correction gastropathy induced by nonsteroidal anti-inflammatory drugs

Hladkykh

2017

Rev Clin Pharm Drug Ther

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Today the problem of prevention and treatment of gastropathy associated with nonsteroidal anti-inflammatory drugs has not lost its relevance. In order to reduce the ulcerogenicity of non-steroidal anti-inflammatory drugs, it is classically accepted to supplement the therapy scheme with preparations of other pharmacological groups - antacids, alginates, M-cholinoblockers, gastrin receptor antagonists, H2-histamine blockers, proton pump inhibitors, synthetic analogues of prostaglandins or stimulators of their synthesis, reparants, gastroprotectors. Nowadays, it was suggested I was suggested the use of drugs which have pharmacological properties polyvector (vinboron, thiotriazoline et al.). Also, the scientists started of combined preparations “NSAIDs + drugs other pharmacological groups” - indotril (indomethacin + thiotriazoline) diklokor (diclofenac + quercetin) Artrotek (diclofenac sodium + misoprostol) dueksis (ibuprofen + famotidine) vimovo (naproxen + esomeprazole) aksorid (ketoprofen + omeprazole) tioaspekard (thiotriazoline + ACK) aspifat (ACK + sucralfate), Alka-Zelttser® (ACK + sodium bicarbonate), and others. The second direction is preventing and improving NSAID gastrotoxicity protrudes improving existing non-steroidal drugs - modification of gaseous molecules (NO, H2S, CO), amino acid derivatives, modulators “effector function” of afferent terminals n. vagus (amtolmetina guatsil) то pairing with nanoparticles biometals (Zn-ibuprofen, Zn-naproxen, Zn-indomethacin). (For citation: Hladkykh FV. Preventive and therapeutic strategies of pharmaco-correction gastropathy induced by nonsteroidal anti-inflammatory drugs. Reviews on Clinical Pharmacology and Drug Therapy. 2017;15(4):14-23. doi: 10.17816/RCF15414-23).

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“…In addition, Hunt and Yuan (2011) related that acid suppression is an important prevention strategy for NSAID-associated gastric ulcer. Gastric lesions caused by NSAIDs can be treated with anti-secretory agents such as proton pump inhibitors or histamine H 2 -receptor antagonists (Satoh and Takeuchi, 2012).…”

Section: Discusssionmentioning

confidence: 99%

Antiulcerogenic activity of the aqueous fraction of Anacardium humile St. Hil (Anacardiaceae)

Luiz-Ferreira¹,

Cola²,

Barbastefano³

et al. 2012

J. Med. Plants Res.

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Anacardium humile St. Hil. is being used in traditional medicine to treat ulcer. The present work evaluated the mechanisms of action involved in the anti-ulcer properties of the aqueous fraction from leaves of A. humile (AHQ). Gastroprotection of A. humile was evaluated in ethanol and piroxicam models. Mechanisms of action such as mucus production, nitric oxide (NO), sulfhydryl compounds (SH) and the anti-secretory action were evaluated. The acetic acid-induced gastric ulcer model was used to evaluate the A. humile healing properties. Results obtained in the ethanol model showed that AHQ provided significant gastroprotection at all the tested doses (50, 100, and 200 mg/kg). Thereby, the following protocols were performed using the dose capable of producing the most effective gastroprotection, which was the AHQ 200 mg/kg (P < 0.001). Moreover, AHQ (200 mg/kg) protected the mucosa from piroxicam-induced damage. Mucus, NO, and SH did not participate on this gastroprotection. AHQ interfere in H + secretion in gastric mucosa, thus exerting an anti-secretory activity. Our results suggest that the gastroprotection and cicatrisation process executed by AHQ occurred due to its anti-secretory activity. This study reinforces its traditional medicinal use. Considering that the current therapies are based on the use of anti-secretory agents, the A. humile arises as a promising alternative antiulcer therapy.

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Management of NSAID/Aspirin-Induced Small Intestinal Damage by GI-Sparing NSAIDs, Anti-Ulcer Drugs and Food Constituents

Cited by 32 publications

References 73 publications

NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

NSAID-Induced Small Intestinal Damage - Roles of Various Pathogenic Factors

Preventive and therapeutic strategies of pharmaco-correction gastropathy induced by nonsteroidal anti-inflammatory drugs

Antiulcerogenic activity of the aqueous fraction of Anacardium humile St. Hil (Anacardiaceae)

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